{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T17:54:20Z","timestamp":1777485260315,"version":"3.51.4"},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,3,27]],"date-time":"2015-03-27T00:00:00Z","timestamp":1427414400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"National Health and Medical Research Council of Australia","award":["GNT1030297"],"award-info":[{"award-number":["GNT1030297"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2015,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Studies were performed to examine the contribution of aldosterone to the pathogenesis of cardiovascular and renal disease in a rodent model of genetic kidney disease. Spironolactone (20\u00a0mg\/kg per day) was administered in water to mixed sex <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>ewis <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>olycystic <jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>idney (<jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content>) rats (<jats:italic>n\u00a0<\/jats:italic>=\u00a020) and control <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>ewis rats (<jats:italic>n\u00a0<\/jats:italic>=\u00a027) from 4 to 12\u00a0weeks of age. At 12\u00a0weeks of age, hypertension was reduced in female <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> rats; systolic blood pressure declined from 226.4\u00a0\u00b1 26.8\u00a0mm<jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>g in untreated rats and to 179.2\u00a0\u00b1\u00a03.2\u00a0mm<jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>g in treated rats (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.018). No similar effect on male or control rats was found. Water consumption and urine volume were significantly greater in <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> animals than in <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>ewis rats, and treatment reduced both variables by ~30% in <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> animals (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). Proteinuria and the urinary protein\u2010to\u2010creatinine ratio were normalized in treated <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> relative to <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>ewis controls, and plasma creatinine levels were significantly reduced by treatment in <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> rats. Spironolactone did not alter kidney morphology in <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> rats (fibrosis or cyst size). Aortic vascular responses to noradrenaline and acetylcholine were sensitized and impaired in the <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01). Aldosterone antagonism did not alter these responses or indicators of aortic structural remodelling. There was no treatment effect on left ventricular hypertrophy or elevated cardiac messenger <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> for \u03b2\u2010myosin\u2010heavy chain and brain natriuretic peptide in the <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> rats. However, perivascular fibrosis and messenger <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> for \u03b1\u2010cardiac actin were normalized by spironolactone in <jats:styled-content style=\"fixed-case\">LPK<\/jats:styled-content> animals relative to <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>ewis controls. In conclusion, we have shown an important blood pressure independent effect whereby inhibition of aldosterone via spironolactone was able to retard both renal and cardiac disease progression in a rodent model of polycystic kidney disease.<\/jats:p>","DOI":"10.1111\/1440-1681.12372","type":"journal-article","created":{"date-parts":[[2015,2,12]],"date-time":"2015-02-12T23:28:06Z","timestamp":1423783686000},"page":"353-360","source":"Crossref","is-referenced-by-count":10,"title":["Protective cardiorenal effects of spironolactone in a rodent model of polycystic kidney disease"],"prefix":"10.1111","volume":"42","author":[{"given":"Thamarasee M","family":"Jeewandara","sequence":"first","affiliation":[{"name":"Australian School of Advanced Medicine Macquarie University Sydney NSW Australia"},{"name":"Sydney Medical School University of Sydney Sydney NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Omar Z","family":"Ameer","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine Macquarie University Sydney NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rochelle","family":"Boyd","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine Macquarie University Sydney NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Benjamin F","family":"Wyse","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine Macquarie University Sydney NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Conor F","family":"Underwood","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine Macquarie University Sydney NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jacqueline K","family":"Phillips","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine Macquarie University Sydney NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,3,27]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040356"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.01340209"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199909023411001"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1586\/14779072.2.3.369"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2008.06.019"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007101079"},{"key":"e_1_2_6_8_1","first-page":"CD008169","article-title":"Spironolactone for hypertension","volume":"8","author":"Batterink J","year":"2010","journal-title":"Cochrane Database Syst. 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